Hemorrhagic shock and tissue injury provoke distinct components of trauma-induced coagulopathy in a swine model.
Introduction: Tissue injury (TI) and hemorrhagic shock (HS) are the major contributors to trauma-induced coagulopathy (TIC). However, the individual contributions of these insults are difficult to discern clinically because they typically coexist. TI has been reported to release procoagulants, while...
| Publicado en: | European Journal of Trauma & Emergency Surgery Vol. 49; no. 2; pp. 1079 - 1090 |
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| Autores principales: | , , , , , , , , , , , , , , , , , , |
| Formato: | research tables/charts Journal Article |
| Publicado: |
Springer Nature
Apr2023
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=163721489&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 163721489 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 18639933 3C05 jtl: European Journal of Trauma & Emergency Surgery issn: 18639933 maglogo: N pubinfo: dt: Apr2023 vid: 49 iid: 2 pid: 237 pub: Springer Nature place: New York, New York artinfo: ui: 163721489 159975865 163721489 163721489 10.1007/s00068-022-02148-x 163721489 ppf: 1079 ppct: 11 formats: fmt: – @attributes: type: T – @attributes: type: P tig: atl: Hemorrhagic shock and tissue injury provoke distinct components of trauma-induced coagulopathy in a swine model. aug: au: Cralley, Alexis L. Moore, Ernest E. Coleman, Julia R. Vigneshwar, Navin Bartley, Matt Kissau, Daniel Eitel, Andrew Hom, Patrick Mitra, Sanchayita Ghasabyan, Arsen Fragoso, Miguel Guo, Zihan Deguchi, Hiroshi Griffin, John H. Cohen, Mitchell J. Silliman, Christopher C. Banerjee, Anirban Hansen, Kirk Sauaia, Angela affil: Department of Surgery, University of Colorado, Aurora, CO, USA sug: subj: Shock, Hemorrhagic Complications Tissue Injuries Trauma Complications Blood Coagulation Disorders Risk Factors Risk Assessment Models, Biological Animal Studies Swine Thrombosis Physiopathology Fibrinolysis Physiology Calcium Blood Thrombelastography Peptide Hydrolases Blood Blood Proteins Analysis Tissue Plasminogen Activator Blood Histones Blood Descriptive Statistics Funding Source ab: Introduction: Tissue injury (TI) and hemorrhagic shock (HS) are the major contributors to trauma-induced coagulopathy (TIC). However, the individual contributions of these insults are difficult to discern clinically because they typically coexist. TI has been reported to release procoagulants, while HS has been associated with bleeding. We developed a large animal model to isolate TI and HS and characterize their individual mechanistic pathways. We hypothesized that while TI and HS are both drivers of TIC, they provoke different pathways; specifically, TI reduces time to clotting, whereas, HS decreases clot strength stimulates hyperfibrinolysis. Methods: After induction of general anesthesia, 50 kg male, Yorkshire swine underwent isolated TI (bilateral muscle cutdown of quadriceps, bilateral femur fractures) or isolated HS (controlled bleeding to a base excess target of − 5 mmol/l) and observed for 240 min. Thrombelastography (TEG), calcium levels, thrombin activatable fibrinolysis inhibitor (TAFI), protein C, plasminogen activator inhibitor 1 (PAI-1), and plasminogen activator inhibitor 1/tissue-type plasminogen activator complex (PAI-1-tPA) were analyzed at pre-selected timepoints. Linear mixed models for repeated measures were used to compare results throughout the model. Results: TI resulted in elevated histone release which peaked at 120 min (p = 0.02), and this was associated with reduced time to clot formation (R time) by 240 min (p = 0.006). HS decreased clot strength at time 30 min (p = 0.003), with a significant decline in calcium (p = 0.001). At study completion, HS animals had elevated PAI-1 (p = 0.01) and PAI-1-tPA (p = 0.04), showing a trend toward hyperfibrinolysis, while TI animals had suppressed fibrinolysis. Protein C, TAFI and skeletal myosin were not different among the groups. Conclusion: Isolated injury in animal models can help elucidate the mechanistic pathways leading to TIC. Our results suggest that isolated TI leads to early histone release and a hypercoagulable state, with suppressed fibrinolysis. In contrast, HS promotes poor clot strength and hyperfibrinolysis resulting in hypocoagulability. pubtype: Academic Journal doctype: research tables/charts Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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